Prospective study of computer-aided detection of colorectal adenomas in hospitalized patients.

BACKGROUND: Adenoma detection with polypectomy during total colonoscopy reduces the incidence of colorectal cancer (CRC) and colorectal cancer-associated mortality. The adenoma detection rate (ADR) is an established quality indicator, which is associated with a decreased risk for interval cancer. An increase in ADR could be demonstrated for several artificially intelligent, real-time computer-aided detection (CADe) systems in selected patients. Most studies concentrated on outpatient colonoscopies. This sector often lacks funds for applying costly innovations like CADe. Hospitals are more likely to implement CADe and information about the impact of CADe in the distinct patient cohort of hospitalized patients is scarce. METHODS: In this prospective, randomized-controlled study, we compared colonoscopies performed with or without computer-aided detection (CADe) system (GI Genius, Medtronic) performed at University Medical Center Schleswig-Holstein, Campus Luebeck. The primary endpoint was ADR. RESULTS: Overall, 232 patients were randomized with n = 122 patients in the CADe arm and n = 110 patients in the control arm. Median age was 66 years (interquartile range 51-77). Indication for colonoscopy was most often workup for gastrointestinal symptoms (88.4%) followed by screening, post-polypectomy and post-CRC surveillance (each 3.9%). Withdrawal time was significantly prolonged (11 vs. 10 min, p = 0.039), without clinical relevance. Complication rate was not different between the arms (0.8% vs. 4.5%; p = 0.072). The ADR was significantly increased in the CADe arm compared to the control (33.6% vs. 18.1%, p = 0.008). ADR increase was particularly strong for the detection in elderly patients aged ≥50 years (OR 6.3, 95% CI 1.7 - 23.1, p = 0.006). CONCLUSION: The use of CADe is safe and increases ADR in hospitalized patients.

Responsiveness to distracting stimuli, though increased in Parkinson's disease, is decreased in asymptomatic PINK1 and Parkin mutation carriers.

Patients with Parkinson's disease (PD) are more sensitive than healthy controls to response-triggering by irrelevant flanking stimuli in speeded choice-response tasks. This increased responsiveness may either indicate a lack of executive control or reflect compensatory efforts to cope with the reduced internal motor drive. Of interest in this context is whether responsiveness is already enhanced in the presymptomatic stage of PD. To address these questions, we studied a group of non-manifesting carriers of heterozygous Parkin and PINK1 mutations while they performed a choice-response task with response-compatible or incompatible flankers. These mutation carriers may be considered a model for pre-clinical PD because the mutant allele leads to a latent nigrostriatal dysfunction and may increase the risk for PD. For comparison, we studied groups of medicated patients with idiopathic PD and of healthy persons age-matched to the mutation carriers and to the patients. Measurements of reaction time, error rate, and the lateralized readiness potential of the EEG provided converging evidence that the mutation carriers were less responsive to distracting flankers than their healthy control group. In contrast, PD patients were more distractible by flankers than their control group, which replicated previous results. Mutation carriers also showed a smaller N2 component of the event-related EEG potential in trials with incompatible flankers relative to their control group, which might indicate reduced inhibitory control. We hypothesize that faulty executive control is the primary deficit, reflected by the reduced N2 component in the mutation carriers. To compensate for this deficit, mutation carriers change their strategy of speed-accuracy trade-off, in order to dampen the excitability of their lateral motor system. Disease progression might prevent symptomatic PD patients from using this compensatory mechanism, leading to increased disinhibition of their lateral motor system.